Anti brain ageing protein- Is it possible?

Researchers from the Yong Loo Lin School of Medicine at the National University of Singapore have made a significant discovery in the quest to understand and potentially combat brain aging. Their study, published in the journal Science Advances, highlights a key protein called DMTF1 (cyclin D-binding myb-like transcription factor 1) that plays a crucial role in maintaining the activity of neural stem cells. These findings suggest that boosting this protein could one day help preserve cognitive functions like memory and learning as people age. 

Neural stem cells are specialized cells in the brain that act as builders and repair crews. Unlike ordinary neurons, they can generate new nerve cells throughout life, a process known as neurogenesis. This is especially vital in the hippocampus, the brain region responsible for forming new memories, supporting learning, and enabling mental flexibility. As we grow older, these stem cells gradually lose their ability to divide and produce new neurons. Scientists believe this decline contributes to common age-related changes, such as slower thinking, weaker memory recall, and difficulty learning new information. 

The brain's natural renewal system becomes less efficient, leading to a progressive loss of cognitive sharpness. The Singapore team's research zeroed in on DMTF1, a transcription factor that functions like a molecular switch. Transcription factors bind to DNA and regulate which genes are activated or suppressed in cells. The study revealed that DMTF1 levels drop significantly in aging neural stem cells, and this reduction is linked to their diminished regenerative capacity. 

In laboratory experiments using aged or "aged" model neural stem cells (including those from human sources and premature aging models), restoring DMTF1 expression revived the cells' ability to proliferate and renew themselves. The cells behaved almost as if they had been partially rejuvenated, regaining much of their youthful division potential.This effect occurs because DMTF1 helps maintain proper DNA accessibility within the cell nucleus. DNA is tightly packed to fit inside cells, but for stem cells to divide or produce proteins needed for regeneration, certain gene regions must "open up" so the cellular machinery can access them. 

DMTF1 promotes this by regulating helper genes like ARID2 and SS18, which are part of the SWI/SNF complex. These genes facilitate chromatin remodeling, making DNA more accessible and activating pathways (such as those involving E2F) that drive cell proliferation. When DMTF1 declines with age, these helper genes become less active, DNA stays compacted, and the stem cells struggle to activate the necessary regeneration programs. 

Restoring DMTF1 reversed this process: the helper genes reactivated, DNA opened appropriately, and the stem cells resumed dividing. While these results are promising, the experiments were conducted primarily in lab-grown cells, not yet in living animals or humans. Translating this to real-world therapies will require more research, including animal studies to confirm benefits in whole brains and to check for side effects. One concern is that stimulating cell division could theoretically raise tumor risks, so any future treatments would need careful design for safety. 

The team aims to identify small molecules or drugs that could safely activate or boost DMTF1 in the brain, but this would involve years of preclinical testing, safety evaluations, and eventual clinical trials. This discovery offers fresh optimism that the aging brain's regenerative decline isn't inevitable or irreversible. By pinpointing a specific molecular mechanism—DMTF1's role in chromatin regulation and stem cell renewal—scientists have a concrete target for future interventions that might help maintain neuron production, preserve memory, enhance thinking speed, and potentially lower the risk of age-related conditions like dementia or Alzheimer's.

The field of brain aging research is advancing rapidly. For instance, in August 2025, a separate team from the University of California, San Francisco identified another protein, FTL1 (ferritin light chain 1), which accumulates in aging brains and contributes to cognitive decline. Reducing FTL1 in aged mice reversed some memory impairments and synaptic changes. These complementary findings highlight growing insights into the proteins driving—or protecting against—brain aging, bringing hope for therapies that could keep minds sharper for longer.

This breakthrough from the NUS team adds to that momentum, showing that targeted restoration of key regulators like DMTF1 could help aging brains hold onto their self-repair abilities. While practical treatments remain years away, the study marks an important step toward understanding—and potentially intervening in—the biology of cognitive aging.